The major emphasis of this research program will be focused on the ocular physiology of the teleost. Prior experiments in our laboratory have shown that the teleost retina which is normally exposed to PO2 in excess of 800 torr, shows no symptoms of oxygen toxicity when exposed to hyperbaric oxygen (HBO) while frog retinas, normally exposed to PO2 no greater than 60 torr, exhibit O2 toxicity when exposed to HBO. Ocular oxygen toxicity has been defined as the attenuation of the electroretinogram and Na-K-Mg ATPase activity. It is generally assumed that cellular O2 toxicity is mediated through the formation of O2- which in normal tissues can be dismutated by superoxide dismutase (SOD). A comparative study of the distribution of SOD as it relates to oxygen partial pressure and oxidative metabolism of retinal tissue will allow us to speculate on the importance of this enzyme in protection against O2 toxicity. In order to correlate the Na-K-Mg ATPase and SOD data, precise intraretinal oxygen profiles will have to be determined. To further verify the role of SOD as a protective agent against O2 toxicity studies on enzyme induction in retinal tissue following HBO will be undertaken. Photo-induced free radical formation has been implicated in cataractogenesis in some species. A comparative study of the effects of sunlight on lens function and metabolism will be undertaken, with specific emphasis on the role of superoxide free radicals. Recent evidence links organophosphate defoliants to lenticular dysfunction and other neuropathies. The exact nature and pharmacological mechanism of this toxicity is unknown and will be investigated.